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Mitochondrial-derived peptides in aging and age-related diseases

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Abstract

A decline in mitochondrial quality and activity has been associated with normal aging and correlated with the development of a wide range of age-related diseases. Here, we review the evidence that a decline in the levels of mitochondrial-derived peptides contributes to aging and age-related diseases. In particular, we discuss how mitochondrial-derived peptides, humanin and MOTS-c, contribute to specific aspects of the aging process, including cellular senescence, chronic inflammation, and cognitive decline. Genetic variations in the coding region of humanin and MOTS-c that are associated with age-related diseases are also reviewed, with particular emphasis placed on how mitochondrial variants might, in turn, regulate MDP expression and age-related phenotypes. Taken together, these observations suggest that mitochondrial-derived peptides influence or regulate a number of key aspects of aging and that strategies directed at increasing mitochondrial-derived peptide levels might have broad beneficial effects.

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Acknowledgments

This work was supported by an Ellison/AFAR Postdoctoral Fellowship in Aging Research Program to SK.

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Authors and Affiliations

  1. The Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA, 90089-0191, USA

    Su-Jeong Kim, Brendan Miller, Hiroshi Kumagai, Ana R. Silverstein, Melanie Flores & Kelvin Yen

  2. Institute of Health and Sports Science & Medicine, Juntendo University, Inzai, Chiba, Japan

    Hiroshi Kumagai

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  1. Su-Jeong Kim
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SK, BM, HK, AS, MF, and KY all participated in the writing of this manuscript.

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Correspondence to Su-Jeong Kim.

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Kim, SJ., Miller, B., Kumagai, H. et al. Mitochondrial-derived peptides in aging and age-related diseases. GeroScience 43, 1113–1121 (2021). https://doi.org/10.1007/s11357-020-00262-5

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